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All these findings indicate that RUNX2 mutation can reduce the osteogenic capacity of dental follicle cells through inhibiting osteoblast-associated genes, thereby disturbing alveolar bone formation, which serves as a motive force for tooth eruption
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these data indicated that miR-23b was involved in TNF-alpha-mediated reduction of bone marrow mesenchymal stem cell osteogenesis by targeting runx2.
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that cross-talk between cAMP/PKA signaling and RUNX2 promotes a malignant phenotype of glioma cells
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Study identified RUNX2 to be targeted by miR-217 which directly bound to RUNX2 mRNA and inhibited its expression in bladder cancer cells. Also, findings demonstrated that RUNX2 expression was upregulated by hsa_circ_0000144. Moreover, rescue assays demonstrated that RUNX2 was a downstream effector molecule of hsa_circ_0000144/miR-217 network. These results revealed the oncogenic role of RUNX2 in bladder neoplasm.
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In summary, these results reveal that PTHLH expression is a poor prognosis marker in head and neck squamous cell carcinoma patients, and RUNX2-PTHLH axis contributes to head and neck squamous cell carcinoma tumor growth.
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Knockdown of RUNX2 significantly inhibited TE-1 and EC-109 cell viability, repressed TE-1 cell migration and invasion, and increased TE-1 cell apoptosis and were associated with the activation of the PI3K/AKT and ERK pathways.
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Results show that RUNX2 gene silencing increased gemcitabine (GEM) sensitivity of p53mutated pancreatic cancer (PaCa) MiaPaCa2 spheres suggesting that RUNX2 is involved in PaCa-GEM resistance in presence of mutated p53.
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Runx2 overexpression effectively decreased TNF-alpha-induced Bax and cleaved caspase-3 expression levels
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RUNX2 is one of the promising molecular targets for the treatment of the patients with pancreatic cancer regardless of their p53 status[review]
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we identified a novel missense mutation of RUNX2 in 2 patients by Whole exome sequencing and showed potential correlations between facial phenotypes and missense mutations in Runt domain through a mini-meta analysis.
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Mutant Runx2 regulates amelogenesis and osteogenesis through a miR-185-5p-Dlx2 axis.
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Results show that RUNX2 is highly expressed in bladder cancer tissues and are negatively correlated with miR-154 levels. This is likely through miR-154 binding the 3'-UTR of RUNX2 mRNA, promoting its degradation.
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Results identified a novel mutation besides the previously known in one patient with cleidocranial dysplasia (CCD). G462X mutation in exon 8 is located in the C-terminus of proline/serine/threonine-rich (PST) domain. It might reduce the Runx2 transacting activity, lower the protein stability, downgrade the expression of bone marker genes, and eventually diminish osteoblast differentiation in CCD patients.
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Findings reveal a novel mechanism that Runx2 is transcriptionally regulated by HSP90 via the AKT/GSK-3beta/beta-catenin signaling pathway, and by which leads to apoptosis of osteosarcoma cells.
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Increased baseline gene expressions of RUNX2, p21 and caspase 3 in the peripheral blood might predict better responses to methotrexate therapy.
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Study identifies a novel missense mutation (c.895 T>C, Y299H) in exon 5 of Runx2 gene in patients with cleidocranial dysplasia (CCD). This mutation results in an amino acid change at codon 895 (P.Tyr 299 His.) from a tryptophan codon (TAT) to a histidine codon (CAT).
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miR-539 functions as a tumor suppressor in colorectal cance, at least in part, by targeting RUNX2.
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These results indicate activation of DLX5 and RUNX2 via its distal promoter represents a unique feature of GFs, and is important for ECM regulation. Down-regulation of these transcription factors in PAFs could be associated with their property to degrade collagen, which may impact on the process of periodontitis.
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down-regulated miR-143-5p promotes the differentiation of DPSCs into odontoblasts by enhancing Runx2 expression via the OPG/RANKL signaling pathway.
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Three novel mutations (R193G, 258fs, Y400X) in cleidocranial dysplasia.
